PDF(Pubmed)
Abstract：
UNASSIGNED: Increased blood pressure variability (BPV) is a risk factor for cerebral small vessel disease (CSVD) and neurodegeneration, independent of age and average blood pressure, particularly in apolipoprotein E4 (APOE4) carriers. However, it remains uncertain whether BPV elevation is a cause or a consequence of vascular brain injury, or to what degree injury to the central autonomic network (CAN) may contribute to BPV-associated risk in APOE4 carriers.
UNASSIGNED: Independently living older adults (n=70) with no history of stroke or dementia were recruited from the community and underwent 5 minutes of resting beat-to-beat blood pressure monitoring, genetic testing, and brain MRI. Resting BPV, APOE genotype, CSVD burden on brain MRI, and resting state CAN connectivity by fMRI were analyzed. Causal mediation and moderation analysis evaluated BPV and CAN effects on CSVD in APOE4 carriers (n=37) and non-carriers (n=33).
UNASSIGNED: Higher BPV was associated with the presence and extent of CSVD in APOE4 carriers, but not non-carriers, independent of CAN connectivity (B= 18.92, P= .02), and CAN connectivity did not mediate the relationship between BPV and CSVD. In APOE4 carriers, CAN connectivity moderated the relationship between BPV and CSVD, whereby BPV effects on CSVD were greater in those with lower CAN connectivity (B= 36.43, P= .02).
UNASSIGNED: Older APOE4 carriers with higher beat-to-beat BPV exhibit more extensive CSVD, independent of average blood pressure, and the strength of CAN connectivity does not mediate these effects. Findings suggest increased BPV is more likely a cause, not a consequence, of CSVD. BPV is more strongly associated with CSVD in APOE4 carriers with lower rsCAN connectivity, suggesting CAN dysfunction and BPV elevation may have synergistic effects on CSVD. Further studies are warranted to understand the interplay between BPV and CAN function in APOE4 carriers.
UNASSIGNED: Independently living older adults (n=70) with no history of stroke or dementia were recruited from the community and underwent 5 minutes of resting beat-to-beat blood pressure monitoring, genetic testing, and brain MRI. Resting BPV, APOE genotype, CSVD burden on brain MRI, and resting state CAN connectivity by fMRI were analyzed. Causal mediation and moderation analysis evaluated BPV and CAN effects on CSVD in APOE4 carriers (n=37) and non-carriers (n=33).
UNASSIGNED: Higher BPV was associated with the presence and extent of CSVD in APOE4 carriers, but not non-carriers, independent of CAN connectivity (B= 18.92, P= .02), and CAN connectivity did not mediate the relationship between BPV and CSVD. In APOE4 carriers, CAN connectivity moderated the relationship between BPV and CSVD, whereby BPV effects on CSVD were greater in those with lower CAN connectivity (B= 36.43, P= .02).
UNASSIGNED: Older APOE4 carriers with higher beat-to-beat BPV exhibit more extensive CSVD, independent of average blood pressure, and the strength of CAN connectivity does not mediate these effects. Findings suggest increased BPV is more likely a cause, not a consequence, of CSVD. BPV is more strongly associated with CSVD in APOE4 carriers with lower rsCAN connectivity, suggesting CAN dysfunction and BPV elevation may have synergistic effects on CSVD. Further studies are warranted to understand the interplay between BPV and CAN function in APOE4 carriers.
摘要：
■血压变异性（BPV）增加是脑小血管疾病（CSVD）和神经变性的危险因素，与年龄和平均血压无关，特别是载脂蛋白E4（APOE4）携带者。然而,尚不确定BPV升高是血管脑损伤的原因还是结果，或对中央自主网络（CAN）的损伤程度可能导致APOE4携带者的BPV相关风险。
■从社区招募了无中风或痴呆病史的独立生活的老年人（n=70），并进行了5分钟的静息搏动式血压监测，基因检测,和脑部MRI。静息BPV,APOE基因型,脑MRI的CSVD负担，通过fMRI分析静息状态CAN的连通性。因果调解和适度分析评估了APOE4携带者（n=37）和非携带者（n=33）中BPV和CAN对CSVD的影响。
■较高的BPV与APOE4携带者中CSVD的存在和程度有关，但不是非携带者，独立于CAN连接（B=18.92，P=0.02），CAN连接并没有介导BPV和CSVD之间的关系。在APOE4运营商中，CAN连接调节了BPV和CSVD之间的关系，其中BPV对CSVD的影响在CAN连通性较低的人群中更大（B=36.43，P=.02）。
■BPV较高的较旧的APOE4携带者表现出更广泛的CSVD，独立于平均血压，CAN连接的强度并不能调节这些影响。研究结果表明，BPV增加更有可能是原因，不是后果,CSVD。在rsCAN连通性较低的APOE4运营商中，BPV与CSVD的相关性更强，提示CAN功能障碍和BPV升高可能对CSVD有协同作用。需要进一步研究以了解APOE4载体中BPV和CAN功能之间的相互作用。
■从社区招募了无中风或痴呆病史的独立生活的老年人（n=70），并进行了5分钟的静息搏动式血压监测，基因检测,和脑部MRI。静息BPV,APOE基因型,脑MRI的CSVD负担，通过fMRI分析静息状态CAN的连通性。因果调解和适度分析评估了APOE4携带者（n=37）和非携带者（n=33）中BPV和CAN对CSVD的影响。
■较高的BPV与APOE4携带者中CSVD的存在和程度有关，但不是非携带者，独立于CAN连接（B=18.92，P=0.02），CAN连接并没有介导BPV和CSVD之间的关系。在APOE4运营商中，CAN连接调节了BPV和CSVD之间的关系，其中BPV对CSVD的影响在CAN连通性较低的人群中更大（B=36.43，P=.02）。
■BPV较高的较旧的APOE4携带者表现出更广泛的CSVD，独立于平均血压，CAN连接的强度并不能调节这些影响。研究结果表明，BPV增加更有可能是原因，不是后果,CSVD。在rsCAN连通性较低的APOE4运营商中，BPV与CSVD的相关性更强，提示CAN功能障碍和BPV升高可能对CSVD有协同作用。需要进一步研究以了解APOE4载体中BPV和CAN功能之间的相互作用。
